Interstitial pneumonia and diffuse alveolar damage in domestic animals

Abstract

Classification of pneumonia in animals has been controversial, and the most problematic pattern is interstitial pneumonia. This is true from the gross and histologic perspectives, and also from a mechanistic point of view. Multiple infectious and noninfectious diseases are associated with interstitial pneumonia, all of them converging in the release of inflammatory mediators that generate local damage and attract inflammatory cells that inevitably trigger a second wave of damage. Diffuse alveolar damage is one of the more frequently identified histologic types of interstitial pneumonia and involves injury to alveolar epithelial and/or endothelial cells, with 3 distinct stages. The first is the “exudative” stage, with alveolar edema and hyaline membranes. The second is the “proliferative” stage, with hyperplasia and reactive atypia of type II pneumocytes, infiltration of lymphocytes, plasma cells, and macrophages in the interstitium and early proliferation of fibroblasts. These stages are reversible and often nonfatal. If damage persists, there is a third “fibrosing” stage, characterized by fibrosis of the interstitium due to proliferation of fibroblasts/myofibroblasts, persistence of type II pneumocytes, segments of squamous metaplasia of alveolar epithelium, plus inflammation. Understanding the lesion patterns associated with interstitial pneumonias, their causes, and the underlying mechanisms aid in accurate diagnosis that involves an interdisciplinary collaborative approach involving pathologists, clinicians, and radiologists.

Obesity fosters severe disease outcomes in a mouse model of coronavirus infection associated with transcriptomic abnormalities

“…[47][48][49][50] DAD represents injury to type I pneumocytes or endothelial cells in the alveolar septa and is characterized by inflammation in the alveolus and alveolar septa and type II pneumocyte hyperplasia. [51][52][53] Although we observed no differences in composite lung pathology between lean and obese infected groups (Figure 3A,C), we did identify type II pneumocyte hyperplasia and inflammation of alveoli and alveolar septa in C57BL/6 N and C3H/ HeJ (Figure 4) mice, consistent with DAD, confirming the validity of our MHV-1 infection models for studying COVID-19 pathogenesis.…”

Hamsters are a model for post-COVID-19 alveolar regeneration mechanisms: an opportunity to understand post-acute sequelae of SARS-CoV-2

“…Thus, the fibrosis could be promoted by the prolonged presence of an unfavorably polarized inflammatory response. In addition to macrophages, AT2 cells can promote a pro-fibrotic microenvironment by activating local fibroblasts to become myofibroblasts via paracrine signaling, as demonstrated in vitro 45,61,62 . This process was initiated by an induction of an EMT process in the AT2 cells 53,62 .…”

“…7 L ). Finally, we investigated the expression of genes involved in angiogenesis, since this process is upregulated in late phases of DAD, in the context of fibrosis 45 . A small number of cells within the AT1/ADI cluster at 5 dpi and a higher number of cells within the AT1/ADI and ADI clusters at 14 dpi revealed high positive scores for angiogenesis hallmark genes ( Fig.…”

Characterization of Macroscopic and Microscopic Lesions of the Respiratory System of Guinea Pig (Cavia Porcellus) in Colombian Production Systems

“…The remaining pneumonic patterns presented percentages less than 1% (n ≤ 2). Two individuals presented interstitial lung disease (diffuse alveolar damage) in exudative stage; this nding is attributed to ventilation-induced lung injury in the euthanasia procedure 11 . In the study, no evidence of bronchointerstitial pneumonic patterns was found.…”